These symptoms are associated with changes in the architecture of the lung. The air sacs, which usually inflate with air during breathing as they loose their elasticity, becoming rigid and unable to inflate. The lung becomes inflamed and increases its mucus production, which further inhibits gas exchange, and prevents the patient's ability to be physically active.

Although COPD is a leading cause of morbidity and mortality worldwide, there is currently no cure for the disease. Providing patients with concentrated oxygen therapy and instruction on breathing techniques increases survival rates.

In a new study published in Disease Models & Mechanisms (DMM), dmm.biologists.org, collaborative findings by European researchers demonstrate that an antioxidant protein, sestrin, triggers molecular pathways that induce some of the critical lung changes associated with COPD. By genetically inactivating this protein, they were able to improve the elastic features of the lung in a mouse model of emphysema. These authors believe that by inhibiting the antioxidant sestrin protein, they prevent the accelerated degradation of elastic fibers within the lung. This suggests that patients with COPD could benefit from treatment with drugs that block sestrin function.

Although sestrin is an antioxidant protein, the authors found that this characteristic of the protein is not likely to influence its effects on COPD progression in the lung. The negative effects of sestrin on lung elasticity results from its suppression of genes whose products maintain elastin. Elastin makes the lung flexible so that it can expand and contract. Without elastin fibers, the lung becomes rigid and increasingly unable to provide for gas exchange.

The report, titled 'Inactivation of sestrin 2 induces TGF-beta signalling and partially rescues pulmonary emphysema in a mouse model of COPD' was written by Frank Wempe, Silke De-Zolt, Thorsten Bangsow and Harald von Melchner at the University of Frankfurt Medical School, Nirmal Parajuli, Rio Dumitrascu and Norbert Weismann at the University of Giessen Lung Center, Anja Sterner-Kock at the Institute of Veterinary Pathology in Germany and Katri Koli and Jorma Keski-Oja at the University of Helsinki in Finland. The study will be published in the March/April issue of 2010 (Vol 3/Issue 3-4) of the research journal, Disease Models & Mechanisms (DMM), published by The Company of Biologists, a non-profit based in Cambridge, UK.

About Disease Models & Mechanisms:

Disease Models & Mechanisms (DMM) is a new research journal publishing both primary scientific research, as well as review articles, editorials, and research highlights. The journal's mission is to provide a forum for clinicians and scientists to discuss basic science and clinical research related to human disease, disease detection and novel therapies. DMM is published by the Company of Biologists, a non-profit organization based in Cambridge, UK.

The Company also publishes the international biology research journals Development, Journal of Cell Science, and the Journal of Experimental Biology. In addition to financing these journals, the Company provides grants to scientific societies and supports other activities including travelling fellowships for junior scientists, workshops and conferences. The world's poorest nations receive free and unrestricted access to the Company's journals.

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